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Article: High-mobility group A (HMGA) genes: from solid to liquid tumours?

Boultwood, J / Wainscoat, J S

2005 Volume 19, Issue 2, Page(s) 195–196

MeSH term(s)	HMGA Proteins/genetics ; Humans ; Leukemia/genetics ; Neoplasms/genetics
Chemical Substances	HMGA Proteins
Language	English
Publishing date	2005-02
Publishing country	England
Document type	Journal Article
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/sj.leu.2403606
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Article ; Online: Haploinsufficiency of ribosomal proteins and p53 activation in anemia: Diamond-Blackfan anemia and the 5q- syndrome.

Boultwood, Jacqueline / Pellagatti, Andrea / Wainscoat, James S

Advances in biological regulation

2012 Volume 52, Issue 1, Page(s) 196–203

MeSH term(s)	Anemia, Diamond-Blackfan/genetics ; Anemia, Diamond-Blackfan/metabolism ; Chromosomes, Human, Pair 5/genetics ; Chromosomes, Human, Pair 5/metabolism ; Cri-du-Chat Syndrome/genetics ; Cri-du-Chat Syndrome/metabolism ; Humans ; Models, Theoretical ; Ribosomal Proteins/genetics ; Ribosomal Proteins/metabolism ; Trisomy/genetics ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Ribosomal Proteins ; Tumor Suppressor Protein p53
Language	English
Publishing date	2012-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2667413-0
ISSN	2212-4934 ; 2212-4926
ISSN (online)	2212-4934
ISSN	2212-4926
DOI	10.1016/j.advenzreg.2011.09.008
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Article ; Online: 5q- syndrome.

Boultwood, Jacqueline / Pellagatti, Andrea / Wainscoat, James S

Current pharmaceutical design

2012 Volume 18, Issue 22, Page(s) 3180–3183

Abstract: In recent years we have gained great insight into the molecular pathogenesis of the 5q- syndrome, the most distinct of all the myelodysplastic syndromes. It is now recognized that p53 activation, caused by haploinsufficiency for the ribosomal gene RPS14 ( ...

Abstract	In recent years we have gained great insight into the molecular pathogenesis of the 5q- syndrome, the most distinct of all the myelodysplastic syndromes. It is now recognized that p53 activation, caused by haploinsufficiency for the ribosomal gene RPS14 (mapping to the commonly deleted region), is the probable cause of the erythroid defect in the 5q- syndrome. A mouse model of the human 5q- syndrome has been generated by large-scale deletion of the Cd74-Nid67 interval (containing Rps14) and the crossing of these '5q- mice' with p53-deficient mice ameliorated the erythroid progenitor defect. Recent evidence suggests that haploinsufficiency of the microRNA genes miR-145 and miR-146a may contribute to the thrombocytosis seen in the 5q- syndrome. Emerging data shows that p53 mutation may play a role in disease progression.
MeSH term(s)	Anemia, Macrocytic/genetics ; Anemia, Macrocytic/physiopathology ; Animals ; Chromosome Deletion ; Chromosomes, Human, Pair 5/genetics ; Disease Models, Animal ; Disease Progression ; Erythroid Precursor Cells/pathology ; Haploinsufficiency ; Humans ; Mice ; MicroRNAs/genetics ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/physiopathology ; Ribosomal Proteins/genetics ; Tumor Suppressor Protein p53/genetics
Chemical Substances	MIRN145 microRNA, human ; MIRN146 microRNA, human ; MicroRNAs ; RPS14 protein, human ; Ribosomal Proteins ; Tumor Suppressor Protein p53
Language	English
Publishing date	2012-04-19
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/1381612811209023180
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Article: Gene silencing by DNA methylation in haematological malignancies.

Boultwood, Jacqueline / Wainscoat, James S

British journal of haematology

2007 Volume 138, Issue 1, Page(s) 3–11

Abstract: The past decade has seen an explosion of interest in the epigenetics of cancer, with an increasing understanding that this form of genomic modification plays a critical role in pathogenesis. The malignant phenotype results from a step-wise increase of ... ...

Abstract	The past decade has seen an explosion of interest in the epigenetics of cancer, with an increasing understanding that this form of genomic modification plays a critical role in pathogenesis. The malignant phenotype results from a step-wise increase of both genetic abnormalities and epigenetic modifications, leading to dysregulation of critical genes controlling cell growth, differentiation and apoptosis. The methylation of CpG islands within gene promoters is a major epigenetic transcriptional control mechanism that is frequently dysregulated in human cancer. This phenomenon (methylation of CpG islands) plays a critical role in the transcriptional silencing of tumour suppressor genes in cancer and has prompted the development and testing of several demethylating agents aimed at reversing this process. Clinical trials using epigenetically targeted therapies have yielded particularly promising results in the myelodysplastic syndromes (MDS), in which tumour suppressor gene silencing by promoter methylation is a frequent event. Several genes and gene pathways disrupted by aberrant CpG island methylation have now been identified in haematological malignancies, the most frequently studied being the cell cycle inhibitors p16 (now termed CDKN2A; mostly methylated in lymphoid malignancy) and p15 (now termed CDKN2B; commonly methylated in lymphoid and myeloid malignancies). This review will discuss the role that aberrant gene silencing by promoter hypermethylation plays in the molecular pathogenesis of haematological malignancies and assess the clinical potential of demethylating agents for the management of patients.
MeSH term(s)	CpG Islands ; DNA Methylation ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Genes, Tumor Suppressor ; Hematologic Neoplasms/genetics ; Humans ; Promoter Regions, Genetic
Language	English
Publishing date	2007-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/j.1365-2141.2007.06604.x
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Article ; Online: Inner solar system material discovered in the Oort cloud.

Meech, Karen J / Yang, Bin / Kleyna, Jan / Hainaut, Olivier R / Berdyugina, Svetlana / Keane, Jacqueline V / Micheli, Marco / Morbidelli, Alessandro / Wainscoat, Richard J

Science advances

2016 Volume 2, Issue 4, Page(s) e1600038

Abstract: ... from the Oort cloud that is physically similar to an inner main belt rocky S-type asteroid. Recent ...

Abstract	We have observed C/2014 S3 (PANSTARRS), a recently discovered object on a cometary orbit coming from the Oort cloud that is physically similar to an inner main belt rocky S-type asteroid. Recent dynamical models successfully reproduce the key characteristics of our current solar system; some of these models require significant migration of the giant planets, whereas others do not. These models provide different predictions on the presence of rocky material expelled from the inner solar system in the Oort cloud. C/2014 S3 could be the key to verifying these predictions of the migration-based dynamical models. Furthermore, this object displays a very faint, weak level of comet-like activity, five to six orders of magnitude less than that of typical ice-rich comets on similar Orbits coming from the Oort cloud. For the nearly tailless appearance, we are calling C/2014 S3 a Manx object. Various arguments convince us that this activity is produced by sublimation of volatile ice, that is, normal cometary activity. The activity implies that C/2014 S3 has retained a tiny fraction of the water that is expected to be present at its formation distance in the inner solar system. We may be looking at fresh inner solar system Earth-forming material that was ejected from the inner solar system and preserved for billions of years in the Oort cloud.
MeSH term(s)	Evolution, Planetary ; Extraterrestrial Environment ; Meteoroids ; Planets ; Solar System
Language	English
Publishing date	2016-04
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.1600038
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Article: Detection and quantitation of circulating Plasmodium falciparum DNA by polymerase chain reaction.

Gal, Shira / Wainscoat, James S

Methods in molecular biology (Clifton, N.J.)

2006 Volume 336, Page(s) 155–162

Abstract: This chapter describes the application of polymerase chain reaction (PCR) for the detection and quantitation of Plasmodium falciparum DNA in the plasma of malaria-infected individuals. The procedure includes the following protocols: plasma sample ... ...

Abstract	This chapter describes the application of polymerase chain reaction (PCR) for the detection and quantitation of Plasmodium falciparum DNA in the plasma of malaria-infected individuals. The procedure includes the following protocols: plasma sample preparation, DNA extraction, detection of P. falciparum DNA in the plasma by nested PCR, and quantitation of P. falciparum DNA in the plasma by real-time PCR technology.
MeSH term(s)	Animals ; DNA/analysis ; DNA/metabolism ; Humans ; Malaria/blood ; Malaria/parasitology ; Plasmodium falciparum/metabolism ; Polymerase Chain Reaction/methods ; Reverse Transcriptase Polymerase Chain Reaction/methods ; Temperature ; Time Factors
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2006
Publishing country	United States
Document type	Journal Article
ISSN	1064-3745
ISSN	1064-3745
DOI	10.1385/1-59745-074-X:155
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Article ; Online: Increasing generations in captivity is associated with increased vulnerability of Tasmanian devils to vehicle strike following release to the wild.

Grueber, Catherine E / Reid-Wainscoat, Elizabeth E / Fox, Samantha / Belov, Katherine / Shier, Debra M / Hogg, Carolyn J / Pemberton, David

Scientific reports

2017 Volume 7, Issue 1, Page(s) 2161

Abstract: Captive breeding of threatened species, for release to the wild, is critical for conservation. This strategy, however, risks producing captive-raised animals with traits poorly suited to the wild. We describe the first study to characterise accumulated ... ...

Abstract	Captive breeding of threatened species, for release to the wild, is critical for conservation. This strategy, however, risks producing captive-raised animals with traits poorly suited to the wild. We describe the first study to characterise accumulated consequences of long-term captive breeding on behaviour, by following the release of Tasmanian devils to the wild. We test the impact of prolonged captive breeding on the probability that captive-raised animals are fatally struck by vehicles. Multiple generations of captive breeding increased the probability that individuals were fatally struck, a pattern that could not be explained by other confounding factors (e.g. age or release site). Our results imply that long-term captive breeding programs may produce animals that are naïve to the risks of the post-release environment. Our analyses have already induced changes in management policy of this endangered species, and serve as model of productive synergy between ecological monitoring and conservation strategy.
MeSH term(s)	Animals ; Breeding ; Conservation of Natural Resources ; Endangered Species ; Female ; Male ; Marsupialia
Language	English
Publishing date	2017-05-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-02273-3
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Article: Clonality in the myelodysplastic syndromes.

Boultwood, J / Wainscoat, J S

International journal of hematology

2001 Volume 73, Issue 4, Page(s) 411–415

Abstract: The myelodysplastic syndromes (MDSs) comprise a heterogeneous group of stem cell disorders involving cytopenia and dysplastic changes in 3 hematopoietic lineages. Although it is accepted that MDS is a clonal disorder, the exact nature of the involvement ... ...

Abstract	The myelodysplastic syndromes (MDSs) comprise a heterogeneous group of stem cell disorders involving cytopenia and dysplastic changes in 3 hematopoietic lineages. Although it is accepted that MDS is a clonal disorder, the exact nature of the involvement of multipotent stem cells and progenitor cells has not been resolved. Most clonality studies of MDS support the proposal that the primary neoplastic event occurs, in most patients, at the level of a committed myeloid progenitor cell, capable of differentiation into multiple myeloid lineages. The extent of the involvement of T and B lymphocytes in MDS remains controversial. Much of the variation reported may result from disease heterogeneity and technical issues such as skewed methylation patterns occurring in studies analyzing X-chromosome inactivation patterns (XCIP) and possible impurities in lymphocyte preparation. A great deal of the evidence in support of T-lymphocyte involvement in MDS has been generated by XCIP studies, and some of these data need to be treated with caution, especially data from studies in which appropriate controls were omitted. In contrast, B-lymphocyte involvement in some patients with MDS is based on studies using more robust technology including combined immunophenotyping and fluorescence in situ hybridization. Clonality studies involving myeloid and lymphoid cells in MDS have yielded discrepant results with regard to the potential involvement of multipotent (lympho-myeloid) hematopoietic stem cells (HSCs). However, failure to detect a clonal marker in all cells of all lineages does not preclude multipotent-HSC involvement. Some recent studies have produced compelling evidence to show that, in some patients with MDS, the multipotent HSC is the target of the primary neoplastic event. It now seems probable that MDS arises in multipotent HSCs more commonly than previously recognized. Such data not only provide important new insights into the biology of MDS but also may have therapeutic implications. The determination of whether multipotent HSCs are involved in the MDS clone may be important for the use of autologous stem cell transplantation in these patients.
MeSH term(s)	Cell Lineage ; Clone Cells/pathology ; Humans ; Lymphocytes/pathology ; Myelodysplastic Syndromes/pathology ; Myeloid Cells/pathology ; Neoplastic Stem Cells
Language	English
Publishing date	2001-06
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	1076875-0
ISSN	1865-3774 ; 0925-5710 ; 0917-1258
ISSN (online)	1865-3774
ISSN	0925-5710 ; 0917-1258
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Article: The origin of mutant beta-globin genes in human populations.

Wainscoat, J S

Acta haematologica

1987 Volume 78, Issue 2-3, Page(s) 154–158

Abstract: ... studies of the origin and spread of some of the common haemoglobinopathies. The beta S mutation has a wide ...

Abstract	The discovery that mutant beta-globin genes arise on different chromosomal backgrounds has allowed studies of the origin and spread of some of the common haemoglobinopathies. The beta S mutation has a wide geographic distribution and is found on many different haplotypes, suggesting that it has had multiple independent origins. In contrast, the Indian beta 0 deletion thalassaemia has a restricted geographic distribution and is present on a single haplotype, suggesting a single origin. The limited evidence for the beta-thalassaemia mutations indicates that most have had a single origin and have subsequently reached polymorphic frequencies by selection pressure from malaria.
MeSH term(s)	Alleles ; Chromosome Deletion ; Genes ; Globins/genetics ; Haplotypes ; Hemoglobin C/genetics ; Hemoglobin E/genetics ; Hemoglobin, Sickle/genetics ; Humans ; Mutation ; Thalassemia/genetics
Chemical Substances	Hemoglobin, Sickle ; Globins (9004-22-2) ; Hemoglobin C (9008-00-8) ; Hemoglobin E (9034-61-1)
Language	English
Publishing date	1987
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	80008-9
ISSN	1421-9662 ; 0001-5792
ISSN (online)	1421-9662
ISSN	0001-5792
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Article ; Online: Activation of the mTOR pathway by the amino acid (L)-leucine in the 5q- syndrome and other ribosomopathies.

Boultwood, Jacqueline / Yip, Bon Ham / Vuppusetty, Chaitanya / Pellagatti, Andrea / Wainscoat, James S

Advances in biological regulation

2012 Volume 53, Issue 1, Page(s) 8–17

Abstract: Patients with the 5q- syndrome and Diamond-Blackfan anemia (DBA) suffer from a severe macrocytic anemia. The 5q- syndrome and DBA are disorders of aberrant ribosome biogenesis (ribosomopathies) and haploinsufficiency of the ribosomal protein genes RPS14 ... ...

Abstract	Patients with the 5q- syndrome and Diamond-Blackfan anemia (DBA) suffer from a severe macrocytic anemia. The 5q- syndrome and DBA are disorders of aberrant ribosome biogenesis (ribosomopathies) and haploinsufficiency of the ribosomal protein genes RPS14 and RPS19, respectively, underlies the anemia found in these disorders. Erythroblasts obtained from patients with the 5q- syndrome and DBA show impaired mRNA translation and this defect in translation may represent a potential therapeutic target in these ribosomopathies. There are some indications that the amino acid l-leucine, a translation enhancer, may have some efficacy in this group of disorders. Recent studies have shown that l-leucine treatment of zebrafish and murine models of the 5q- syndrome and DBA results in a marked improvement in the anemia. l-leucine treatment of RPS14-deficient and RPS19-deficient erythroblasts and erythroblasts from patients with the 5q- syndrome has been shown to result in an increase in cell proliferation, erythroid differentiation and mRNA translation in culture. l-leucine has been shown to improve hemoglobin levels and transfusion independence in a patient with DBA. l-leucine activates the mTOR (mammalian target of rapamycin) signaling pathway that controls cell growth and mRNA translation. There is evidence to suggest that the promotion of translation via the mTOR pathway by l-leucine is the mechanism that underlies the enhanced erythroid progenitor cell growth and differentiation observed in animal and cellular models of the 5q- syndrome and DBA treated with this amino acid. These data support the rationale for clinical trials of l-leucine as a therapeutic agent for the 5q- syndrome and DBA.
MeSH term(s)	Anemia, Diamond-Blackfan/drug therapy ; Anemia, Diamond-Blackfan/genetics ; Anemia, Diamond-Blackfan/metabolism ; Anemia, Diamond-Blackfan/pathology ; Anemia, Macrocytic/drug therapy ; Anemia, Macrocytic/genetics ; Anemia, Macrocytic/metabolism ; Anemia, Macrocytic/pathology ; Animals ; Chromosome Deletion ; Chromosomes, Human, Pair 5/genetics ; Chromosomes, Human, Pair 5/metabolism ; Erythroblasts/drug effects ; Erythroblasts/metabolism ; Erythroblasts/pathology ; Gene Expression Regulation/drug effects ; Haploinsufficiency ; Humans ; Leucine/metabolism ; Leucine/pharmacology ; Protein Biosynthesis ; Ribosomal Proteins/genetics ; Ribosomal Proteins/metabolism ; Ribosomes/drug effects ; Ribosomes/genetics ; Ribosomes/pathology ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	RPS14 protein, human ; Ribosomal Proteins ; ribosomal protein S19 ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Leucine (GMW67QNF9C)
Language	English
Publishing date	2012-09-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2667413-0
ISSN	2212-4934 ; 2212-4926
ISSN (online)	2212-4934
ISSN	2212-4926
DOI	10.1016/j.jbior.2012.09.002
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